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Systems Neuroscience > Brain and Body Systems > Flashcards

Brain and Body Systems Flashcards

1
Q

draw the flow diagram of CNS<->PNS with notes for each section

A

see notes

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2
Q

what is the purpose of the Peripheral NS?

A

the implement the CNS’ connection with the body/wider world

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3
Q

when is the parasympathetic NS active?

A

during rest and digest when in relaxed state

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4
Q

when is sympathetic nervous system active?

A

during fight or flight/aroused state when there’s a stressor

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5
Q

draw a diagram of the BBB and it’s elements

A

see notes- the image B

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6
Q

why does the brain need so much
vasculature?

A

the brain has high metabolic needs, using about 20% of cardiac output, despite being 2% of body weight.
Because it has very little storage ability glucose and oxygen need to be delivered as and when it’s needed through a dense capillary network

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7
Q

what is the downside of the dense vasculature/constant blood supplied required by the brain?

A

it makes it vulnerable if there’s any interruption, which can quickly was local/wider injury and dysfunction

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8
Q

what is neurovascular coupling

A

whereby neuronal activation triggers increased BF to an area

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9
Q

Neurovascular unit ~

A

BBB

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10
Q

define BBB

A

an interconnected system of neurons, astrocytes, pericytes, vascular cells (endothelial cells)

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11
Q

what are hormones

A

signalling molecules produced by endocrine organs throughout the body and transported around the body via vascular system. Essential for development, physiology and behaviour by regulating systems to maintain desired state

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12
Q

what has overall control of the endocrine system?

A

the brain (with feedback architecture)

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13
Q

what’s the basic flow chart of endocrine/hormone?

A

hypothalamus-> pituitary -> hormones secreted to effect other glands/systems

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14
Q

name 3 differences between hormones and neurotransmitters:

A
  • NTs are faster acting, hormones slower
  • NTs travel shorter distances (along neural networks), whereas hormones can travel throughout the body (via circulatory system)
  • NTs act in the shorter term, whereas hormones have longer term effects
  • NTs have digital actions (on/off), whereas Hormones have analogue (continually variable)
  • NTs tend to have more targeted action, whereas hormones as more diffuse

(overall hormones are able to reach parts of the body NTs can’t access, working through different mechanisms that complement CNS/PNS

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15
Q

Overview of hormones and BBB

A

hormones travel in the blood, so BBB cells have receptors for them in order for hormones from body to trigger neural changes. Hormones produced in the brain can also cross the BBB often to go on to target endocrine receptors in the body. Some BBB cells are autocrine and some paracrine

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16
Q

overall, where does the hypothalamus receive input from?

A

cerebral cortex (including somatosensory cortex), amygdala, hippocampus and visceral sensory input

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17
Q

overall, where does the hypothalamus output to?

A

visceral and somatic motor neurons, neuroendocrine and behavioural pathways

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18
Q

how does the hypothalamus connect/communicate with anterior pituitary?

A

via short BVs (sending releasing hormones for pituitary to release into blood

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19
Q

how does the hypothalamus connect/communicate with posterior pituitary?

A

through neural connections

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20
Q

what diseases are implicated in the connection between brain disease and neurovascular function?

A

diabetes, NT disturbances, stroke, epilepsy

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21
Q

what did a review by Kulshreshthra (2019) show?

A

that CVD risk factors, such as hypertension and cigarette smoking and positively associated with cognitive decline (showing link between CV health and brain function)

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22
Q

what did Barnes (2015) review show?

A

exercise both reduces CVD risk and is protective of cognitive function (indicating link between cardiovascular health and brain health)

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23
Q

what is the proposed mechanism by which cardiovascular health is impacting brain health?

A

many studies have shown changes in circuit function (functional connectivity)

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24
Q

because there is a lack of effective treatments for CNS diseases involving cognitive decline/dementia, it’s important to…

A

look at preventative lifestyle factors to avoid onset

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25
Q

what are the strongest evidenced factors shown to increase the risk of both cognitive decline and dementia?

A
  • TBI
  • mid-life obesity
  • hypertension
  • current smoking cigarettes
  • diabetes
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26
Q

what’s the strongest evidenced factors that reduce the risk of cognitive decline and dementia?

A
  • greater number of years of formal education
  • physical activity
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27
Q

what does the immune system do?

A

senses environmental change in body and co-ordinates a response, including cellular, biochemical, physiological/behaviour changes. It self-regulates and remembers

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28
Q

what are the 3 levels of the immune system?

A
  • Anatomical/Physiological barriers (counts as innate immunity)
  • Innate immunity
  • adaptive immunity
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29
Q

give 2 examples of anatomical/physiological barriers:

A

2 from:
- skin
- ciliary clearance
- low stomach pH
- lysozyme in tears and saliva

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30
Q

what is innate and adaptive immunity further divided into?

A

cellular and humoral

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31
Q

give 3 cells of innate immunity:

A

3 from:
- eosinophils
- macrophage
- mast cells
- dendritic cells
- neutrophils
- natural killer cells

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32
Q

give 2 examples of aspects of innate humoral immunity:

A

2 from:
- complement system
- mannose binding lectin
- antimicrobial peptides
- LPS binding protein
- c-reactive protein

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33
Q

what are the 2 cells of adaptive immunity?

A

T and B cells

34
Q

what are the humoral aspects of adaptive immunity?

A

antibodies

35
Q

define neuroimmunology

A

interaction of immune and nervous systems (CNS controls nervous system and receives feedback)

36
Q

what is psychoimmunology

A

interaction between psychological processes and immune/nervous systems (mind-body connection)

37
Q

outline immunity within the brain

A

the brain has microglia, the resident immune cells, which sense damage/pathogens and trigger larger scale immune responses. It can communicate with body systems via the BBB to launch wider immune response

38
Q

via what routes to te brain and body systems relating to immunity communicate?

A

both direct and indirect routes:
CNS, PNS, BBB (blood), cell-cell communication, cytokines, hormones

39
Q

give 3 examples of glands, hormone they produce and hormone role:

A
  • thyroid gland in neck, releases thyroid hormone, key role in metabolism
  • parathyroids, below thyroid gland, releases parathyroid hormones which regulates blood calcium
  • adrenal glands on kidney, release adrenaline and cortisol, response to stressor/sympathetic response
  • pancreas, releases insulin, blood sugar regulation
  • testis- male sex hormones e.g. testosterone, many roles including sperm production
  • ovaries- female sex hormones, e.g. oestrogen- regulate female reproductive system
40
Q

draw table of hypothalamus-anterior pituitary connections/roles

A

see table in notes

41
Q

draw table of hypothalamus-posterior pituitary roles

A

see table in notes

42
Q

what are the 2 examples of hormone regulation focused on in course?

A

energy balance and stress response

43
Q

what is energy balance in body

A

high or low energy states either motivate feeding or fasting behaviours- promoted/inhibited by the hypothalamus

44
Q

draw an image of the hormones organs involved in energy balance/eating behaviour

A

see notes

45
Q

is ghrelin the only hormone/substance from the gut signalling hunger/feasting behaviour?

A

no e.g. OXM (oxytomodulin)

46
Q

as well as hormonal/mechanoreceptor input to hypothalamus, what else effects energy balance/feeding behaviour?

A

autonomic nervous system actions, e.g. if you’re preparing for physical activity

47
Q

outline the role of the arcuate nucleus of hypothalamus in energy balance

A

key integrator for hormone signalling input, projects to other hypothalamic structures and onwards to cortical and limbic circuits

48
Q

what are the 2 types of regulation of feeding behaviour?

A

homeostatic and hedonic

49
Q

outline homeostatic regulation of feeding behaviour

A

based in hypothalamus (arcuate nucleus and lateral hypothalamus) and signalling the need for food

50
Q

outline the hedonic regulation of feeding behaviour

A

based in mesolimbic regions, signals the want from food with links to pleasure. Specifically dopaminergic signalling from VTA to NAc underlies the hedonic drive

51
Q

draw diagram of hedonic and homeostatic regulation with notes

A

see notes

52
Q

what did Volkow 2009 find? - relate to pathology and obesity

A

that brain reward circuits can be activated by the same hormones that are key for homeostatic regulation. When there is both leptin decrease and ghrelin increase, the hedonic reward circuit has increased sensitivity to food stimuli (fMRI BOLD).
This indicated a pathological aspect of food addiction when these circuits are dysregulated.

  • individuals with obesity have blunted central reward circuit sensitivity to food, whereas primary somatosensory signaling relating to taste/eating is enhanced.
53
Q

what other hormone (than dopamine) has been implicated in the food reward mechanism?

A

oxytocin- released by hypothalamic neurons when food is present (modulates both hedonic and homeostatic pathways)

54
Q

discuss loss of appetite control in obesity

A

chronically high leptin levels (due to high adipose tissue volume) can cause leptin resistance both peripherally and centrally. This is seen in inflammation effecting the BBB function so leptin is unable to cross, hence not being able to send satiety signals. In addition impaired leptin receptor expression are also seen in liver, muscle and adipose with signalling molecules such as NPY which promote hunger going up and POMC which promotes satiety going down.

55
Q

what is the stress response briefly?

A

the ability to mobilise body systems appropriately and rapidly in the event of acute threat- to aid survival

56
Q

what are the 2 primary hormonal pathways activated with the stress response?

A

1) Sympathetic-Adrenal-Medullary pathway (SAM)
2) Hypothalamic-Pituitary Adrenal (HPA) axis

57
Q

what hormone is released by SAM response?

A

adrenaline

58
Q

what hormone is produced by HPA axis?

A

cortisol

59
Q

draw flow diagram of the acute stressor leading to the hormonal stress pathways

A

see needs

60
Q

in the SAM pathway, what projection from the hypothalamus is used to activate sympathetic nervous system?

A

brainstem/spinal cord

61
Q

is adrenaline a hormone or NT?

A

both (acts simultaneously with other SNS effects)

62
Q

how is adrenaline production stopped

A

the absence stressor- does not have direct negative feedback to pituitary/hypothalamus

63
Q

which receptors does adrenaline activate and what are the results of this?

A

look at picture in notes

64
Q

what are the 2 main roles of cortisol?

A

elevate glucose availability and immune suppression

65
Q

overall, how does cortisol elevate glucose availability?

A

increase the breakdown of fat/protein and increase glycogenesis in liver to increase blood sugar levels

66
Q

overall, how does cortisol suppress immunity?

A

reduces allergic reactions and inflammation

67
Q

outline chronic stress

A

stress response systems (HPA/SAM/SNS) are designed to handle transient stressors and resolve quickly in the absence of stressor. However, many people suffer from chronic stress due to the constant presence of stressors, causing long-term activation of HPA and SAM. This causes long term effects on the body such as increased BP from adrenaline or psychological effects such as depression due to reduced serotonin through cortisol’s activity

68
Q

overview stress and CV function/disease

A

brain circuits controlling CV function act via the autonomic nervous system (visceral tissue/muscle e.g. for heart contraction and vasodilation). ANS receives input from cortical and subcortical systems responsible for a wide range of psychological and psychological activities

69
Q

draw the flow diagram of how mental stress can lead to CVD

A

see notes

70
Q

overview the example of Alzheimer’s Disease regarding the role of neurovascular function

A

since the 80s it has been believed that vascular disruption was a consequence of cell/synapse loss seen in AD, however, some recent evidence suggests that breakdown of vasculature and NV coupling may occur prior to cellular effects/ amyloid beta plaques and NFTs

71
Q

overview physical activity and cognitive function

A

many function neuroimaging studies show changes in cognitive function/ circuit connectivity following exercise intervention. For example 2017 Wang et al. found 30 mins of moderate intensity aerobic cycling selectivity increased synchrony among many brain regions including those involved in reward/learning/attention etc.

72
Q

draw the flow diagram with risk factors and mechanisms of vascular disease and neurological disease

A

see notes

73
Q

outline research into brain vascular function in diabetes

A
  • a multimodal neuroimaging investigation of brain vascular responses, comparing health control, diabetic and pre-diabetic patients, found a wide range of changes in how blood is delivered to tissue in diabetic and pre-diabetic patients compared to healthy controls.
  • Chhabria et al 2018. used a hyperglycaemic zebrafish model and found that chronically increased blood-glucose impairs NV function
74
Q
A
75
Q

which systems are involved in the interoceptive input to the brain from body systems

A
  • cardiovascular
  • metabolic
  • visceral sensory afferents
  • chemoreceptors in blood vessels
76
Q

give an example of how the heart’s activity is involved in interoception in the brain

A

research found that the brain responds differently to sensory stimuli depending on where in the cardiac cycle the heart is (systole or diastole)

77
Q

how is exercise meant to improve chronic stress?

A

it has been found to alter DA signalling to increase reward-related responses. This buffers the effects of stressors by bolstering the negative feedback from cortisol to hypothalamus/anterior pituitary

78
Q

overview immunity and depression

A

immune responses in the body are associated with altered function in a wide range of brain circuits e.g. inflammation is associated with reduced functional connectivity within corticostriatal circuitry and reduced serotonergic system activity (sickness behaviour), seen in depression, indicating that immune action/inflammation may have a causative role in depression. Hence long-term sickness behaviour and depression- similar (e.g. in chronic inflammation)

79
Q

overview sickness behaviour

A
  • an example of how immune system in body interacts with neural circuits
  • brain produces behaviour such as listlessness, sleepiness to promote recovery
  • pro-inflammatory cytokines are thought to be closely related to sickness behaviour
  • the behaviour’s purpose is to conserve energy which can be redirected to immune cells to encourage healing
  • some evidence suggests that changes in mood associated with sickness behaviour are due to immune modulation of serotonergic systems
80
Q

outline stress and immune response

A

stress, in particular the activation of HPA axis, increases cortisol, known to suppress immune function (anti-inflammatory), this is adaptive in the short-term, however over longer term prolonged immune suppression can dysregulate immune system e.g. increasing susceptibility to illness.

81
Q

outline the complexities of neurovascular function and feeding behaviours/pathology

A

it is a chicken and egg situation where it is unclear if changes in vasculature e.g. neurovascular uncoupling and BBB breakdown occur prior to pathological trigger (does it breakdown, then causing reduced leptin sensitivity) or whether high adipose then causes genetic changes/leptin insensitivity, leading to inflammation then breakdown of BBB
definitely a positive feedback cycle involved.

82
Q

outline complexities of immune activation/inflammation and brain activity

A

inflammation an altered connectivity have been clearly shown, e.g. the changes in corticostriatal circuits accompanied alongside inflammation and linked to depressive symptoms. as well as altered connectivity in cognitive/sensory/motor networks seen in older adults without dementia. The causation/initiating factor is unclear, does the CNS functional change affect peripheral immunity or does peripheral immunity alter CNS functional connections?

Systems Neuroscience (3 decks)

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